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  • Title: Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells.
    Author: Park HS, Chun JN, Jung HY, Choi C, Bae YS.
    Journal: Cardiovasc Res; 2006 Dec 01; 72(3):447-55. PubMed ID: 17064675.
    Abstract:
    OBJECTIVE: We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs). METHODS AND RESULTS: Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-kappaB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively. CONCLUSIONS: Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner.
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